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  • Michele Curatolo

Explaining "pain sensitization" to patients


 

In this blog, I discuss how to explain to patients a crucial determinant of their pain: "sensitization".

Pain is not only the result of a signal arising from a damaged tissue, such as an inflamed joint or a degenerated disk of the back. As discussed in a previous blog, the pain experience is the ultimate result of processes that occur at different sites of the pathways that are involved in the generation, transmission, elaboration, and perception of pain: the site of injury, nerves that transmit the signal to the spinal cord, and cells within the spinal cord and the brain (neurons and other cell types). In the brain, areas that are responsible for pain perception are connected with areas that elaborate cognition and emotion. Therefore, what we call "pain intensity" is not just the result of the magnitude of the signal arising from the injured area, but of the integration of many processes that occur at all levels of the "pain system".

This notion has revolutionized the way we understand pain, and has therapeutic consequences, as it adds potential sites of intervention that go beyond the treatment of the primary injury.

This is particularly relevant for the many patients for whom there is no cure of the primary injury.

For instance, arthritis cannot be reverted, and there is no treatment that restores a damaged nerve to a pre-injury condition. However, treatments that attenuate processes enhancing the pain signal ("pain sensitization") may be available.

Whenever we are unable to "fix" tissues damage, shifting the goal of the treatment towards a reduction of "pain sensitization" can be beneficial.

How do we convey this information to patients?


"The doctor thinks that my pain is all in my head."

This misunderstanding is very common when health care professionals try to explain the current understanding of pain. Definition that are widely established among scientists, such as "central sensitization" or "nociplastic pain" remain incomprehensible for most patients. And yet, it is essential that patients are aware of the potential causes of their pain. This can be achieved by programs called "pain neuroscience education". However, we first need to gain patient's trust and interest in undergoing such educational sessions.


Let's talk patient's language

I have made good experience with a simple scheme that I am sharing in the figure below. Feel free to use or share it. It explains that, when a pathological change occurs in a tissue, pathways in the peripheral and central nervous system become hyper-active (arrows 1-2). Hyper-activation of neurons and other cells of the nervous system ("glial cells") can occur also without an inciting event (arrow 3): this is the way we currently understand certain chronic pain conditions that are not associated with evident tissue damage, such as fibromyalgia.

Scientists and health care professionals call "sensitization" the hyper-activation described in the figure, and distinguish "peripheral" from "central" sensitization. This distinction is frequently difficult to ascertain in clinical conditions and is hard to understand for patients. I propose to use with patients the collective term "pain sensitization".

When a pathological change occurs in a tissue, such as osteoarthritis, inflammation, fracture, or degeneration, substances that are released in the tissue make nociceptive pathways more likely to be activated. As a result, a stimulus or activity that is normally painless, such as walking or lifting a weight, can generate pain. The signal arrives at the spinal cord and induces changes that increase the excitability of neurons, resulting in further amplification of pain.

It is essential for patient to understand that sensitization is a crucial contributor to their symptoms (text box of the figure). It becomes then easier to explain why, for example, mindfulness may be helpful, as it can work on the hyperactivity of "pain regions" of the brain. Similarly, it can motivate patients to try other treatments of sensitization, such as certain forms of physical therapy, anticonvulsants, medications acting on serotonin/noradrenaline pathways, or psychological treatments.


To summarize:

  • Processes that lead to amplification of the pain signal are of crucial relevance, and can be presented to patients as "pain sensitization". While this is not an official scientific term and can be semantically questioned, it is easier to understand.

  • Gaining patient's trust and openness to understand sensitization is mandatory to allow acceptance of treatments that target sensitization. This is of particular importance for patients who have tissues damage that cannot be cured.

  • Expectation of treatment effect is of essential importance. Therefore, treatments that target sensitization are most likely to be effective if patients understand the rationale.

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